Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute kidney injury (AKI) with evidence of hemolysis is associated with tropical infections. However, pigment-induced AKI can happen with relatively uncommon genetic causes of hemolytic anemia, i.e., glucose 6-phosphate deficiency (G6PD). We share our experience of three such patients whose clinical presentation was similar to jaundice, AKI with hemolysis with suspicion of thrombotic microangiopathy. On evaluation, all had a history of usage of anti-malarial and with G6PD estimation revealing deficient status even during the episode while other tests such as Coomb's test and bone marrow biopsy was normal in all three patients. The kidney biopsy revealed acute tubular necrosis with red blood cell casts and pigments in all the cases. All patients were managed conservatively and showed complete recovery. Thus in tropical countries G6PD deficiency although is not common, should be considered among patients who have received antimalarial drugs presenting as AKI and a detailed hemolytic work-up needs to be carried out as an important cause of preventable recurrent AKI in tropical countries.
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PMID:G6PD deficiency is not an uncommon cause of pigment nephropathy. 3058 69

Coronavirus disease 2019 (COVID-19) is commonly associated with kidney damage, and the angiotensin converting enzyme 2 (ACE2) receptor for SARS-CoV-2 is highly expressed in the proximal tubule cells. Whether patients with COVID-19 present specific manifestations of proximal tubule dysfunction remains unknown. To test this, we examined a cohort of 49 patients requiring hospitalization in a large academic hospital in Brussels, Belgium. There was evidence of proximal tubule dysfunction in a subset of patients with COVID-19, as attested by low-molecular-weight proteinuria (70-80%), neutral aminoaciduria (46%), and defective handling of uric acid (46%) or phosphate (19%). None of the patients had normoglycemic glucosuria. Proximal tubule dysfunction was independent of pre-existing comorbidities, glomerular proteinuria, nephrotoxic medications or viral load. At the structural level, kidneys from patients with COVID-19 showed prominent tubular injury, including in the initial part of the proximal tubule, with brush border loss, acute tubular necrosis, intraluminal debris, and a marked decrease in the expression of megalin in the brush border. Transmission electron microscopy identified particles resembling coronaviruses in vacuoles or cisternae of the endoplasmic reticulum in proximal tubule cells. Among features of proximal tubule dysfunction, hypouricemia with inappropriate uricosuria was independently associated with disease severity and with a significant increase in the risk of respiratory failure requiring invasive mechanical ventilation using Cox (adjusted hazard ratio 6.2, 95% CI 1.9-20.1) or competing risks (adjusted sub-distribution hazard ratio 12.1, 95% CI 2.7-55.4) survival models. Thus, our data establish that SARS-CoV-2 causes specific manifestations of proximal tubule dysfunction and provide novel insights into COVID-19 severity and outcome.
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PMID:SARS-CoV-2 causes a specific dysfunction of the kidney proximal tubule. 3291 78


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